2012 role of ct in detection of plaque

8/11/2019 2012 Role of CT in Detection of Plaque

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Research Article Open Access

Youssef and Budoff, Angiol 2013, 1:2

http://dx.doi.org/10.4172/2329-9495.1000111

Review Article Open Access

Angiology: Open Access

Volume 1 Issue 2 1000111Angiol

ISSN: 2329-9495 AOA, an open access journal

Introduction

Atherosclerotic cardiovascular diseases are still the leading causeo deaths in industrialized Countries and Coronary Artery Disease(CAD) accounts or the majority o this toll [1]. Cardiac events aretypically caused by disruption o coronary plaques where plaquerupture occurs in about two thirds o cases, while the remaining thirdo cases are caused by plaque erosion with subsequent ormation ooccluding thrombus [2]. Tus, a clinically relevant definition o arupture-prone (or what has been termed the vulnerable) plaque, isa lesion that places a patient at risk or uture major adverse cardiacevents, including death, myocardial inarction, or progressive angina.

On the other hand, the histopathological eatures that have beenassociated with vulnerable plaques and dened them, include: 1) A largeeccentric necrotic lipid core, occupying approximately one-quarter othe plaque area [3], 2) A thin brous cap (


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Citation: Youssef G, Budoff M (2013) Role of Computed Tomography Coronary Angiography in the Detection of Vulnerable Plaque, Where Does it

Stand Among Others? Angiol 1: 111. doi: 10.4172/2329-9495.1000111

Page 2 of 8



Modality Mechanism Spatial resolution Strengths Limitations Relevant Studies

Invasive Modalities

Intravascular ultrasound

(IVUS) [8-11]

The intensity of the backscattered

signalis processed into gray scale

differs among different plaque

components

150 m

Provides information on

plaque anatomical features

and composition to lesser

extent [12]

-Invasiveness

-Limited temporalresolution

-Limited spatial resolution

so cannot recognize thin

cap brotheroma (TCFA)

-Gray scale IVUS cannot

accurately differentiate

elements of plaque

composition

-Features of plaquevulnerability include:

eccentric pattern,

echolucent core, positive

remodeling, presence of

thrombi, plaque length,

lumen narrowing and

spotty calcication [13,14]

IVUS-RF (radiofrequency)

analysis e.g. Virtual

histology (VH) [8-11]

RF data are more in direct

relation to the interaction of

ultrasound with tissue

100-200 m

-Ability to differentiate

between 4different tissue

types in plaques; dense

calcium, brous, bro-fatty

and necrotic core [15]

-Identication of TCFA

-Invasiveness


-When compared to

histology, sensitivity,

specicity and predictive

accuracy of VH to

detect necrotic core,

a vulnerability feature

were 67%, 93% and 88%

respectively [16]

-PROSPECT study showeda correlation between

presence of TCFA and

future major adverse

cardiac events (hazard

ratio: 3.35) [17,18]

Palpography

(intravascular

elastography)

[8,10]

Measures the local strain rate of

vessel wall and plaque (brous

plaques are stiffer than lipid-rich

ones) high strain regions denote

more vulnerable plaques

200-400 mIdentication of thin brous

caps

-Invasiveness


-Cardiac motion

Human studies have

shown a strong correlation

between number of highly

deformable plaques

and both the clinical

presentation (ACS Vs.

stable patients) [18]

Intravascular MRI (IV-MRI)

[8]

Calculates the water diffusion

coefcient: lipid-rich < brous

plaques

120 mDetection of plaque

composition-Invasiveness

There was a good

correlation between

MRI and histology with

sensitivity and specicity of

100% and 89% [19]

Angioscopy [8-11]

Direct visualization of the

endothelial surface. The intensity

of the yellow color detected is

used for plaque characterization

200 m

Precise visualization of

plaque surface detecting

disrupted plaques (ulcers,

ssures)

-Invasiveness

-Limited

tissue penetration and

spatial resolution

Number of yellow plaques

were shown to be a strong

predictor of ACS [20]

Optical coherent

tomography (OCT) [8-11]

Light-based imaging, measures

the amplitude of backscattered

light (optical echoes) from a

sample as a function of time

delay

4-20 m

-Highest spatial resolution,

able to resolve thin brous

caps


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Systematic comparison between invasive and non-invasivemodalities or coronary plaque characterization in ex-vivo specimensdemonstrated that CCA and IVUS are reasonably associated withplaque composition and lesion grading according to histopathologicndings, while Optical Frequency Domain Imaging (a secondgeneration o OC) was strongly associated.

Imaging eatures that were associated with advanced lesions were,mixed plaque at CCA, calcication at IVUS and lipid-rich plaqueat OFDI). Moreover, OFDI showed a better diagnostic accuracydifferentiating early rom advanced coronary lesions, with area underthe curve (AUC) o 0.8 compared to AUC o 0.63 and 0.68 or IVUSand CCA respectively [21].

Multi-detector Computed TomographyFirst-generation scanners, or conventional C, utilized a single

X-ray source and single X-ray detector cell. Over the past two decadeswith the tremendous advances in technology, MDC presented abreakthrough in cardiac C imaging technology by 1) increasing thenumber o detector rows rom 4 to 320 thus increasing the coveragein the Z-axis up to 16 cm in a single heart beat with a single gantryrotation, 2) speeding up the gantry rotation, enough to reeze thecardiac motion by capturing images within the relatively brie periodo cardiac diastasis. the use o dual-source MDC system has markedlyimproved the temporal resolution to approximately 85 msec, resultingin a shorter scan time and 3) decreasing the thickness o the detectorsto 0.5-0.625 mm thus increasing the spatial resolution to image sub-

millimeter structures. Tis has allowed more accurate and detailedimaging o coronary plaques morphology and composition.

MDC has caught up with coronary angiography, showing an

excellent diagnostic accuracy in diagnosis o obstructive CAD whencompared to coronary angiography as the gold standard. In a recentmeta-analysis o 188 studies (rom 2004 to 2011), the mean sensitivityand specicity o MDC were 97% and 87% respectively [31].

Role of MDCT in Detection of Vulnerable Plaque;Morphology and Composition

Te potential or MDC evaluation o coronary plaques is

enormous, given its noninvasive nature and its ability to evaluatethe entire coronary arterial tree in contrast to IVUS.MDC can helpdetect the suggested triad o the main eatures associated with plaque

vulnerability namely; positive remodeling, low attenuation (


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conrmed when Pflederer et al. [37] showed a signicantly higher

remodeling index in ACS patients when compared to those with stable

angina (1.6 0.4 Vs. 0.97 0.17, P0.9with

excellent sensitivity and specicity o 100% and 90% respectively [38].

Interestingly, in a recent paper that used coronary artery simulation

models, vessel wall stress concentrations were always predicted to be

higher in the fibrous cap o plaques with positive remodeling compared

to those with negative remodeling independent o the fibrous cap and

the degree o stenosis [39].

Invasive coronary imaging is the gold standard or detection o

disrupted plaques, the angiographic hallmark o complex lesions was

characterized by Ambrose criteria including haziness, ulceration,

intraplaque dye penetration and intraluminal lling deects, theseeatures correlated with both histology and IVUS [40]. Tere are only

scant data regarding the ability o Computed omography Coronary

Angiography (CCA) to identiy eatures o plaque disruption;

ulceration and/orintraplaque dye penetration. When compared to

IVUS, MDC was less accurate or the detection o plaque disruption

in coronary arteries; sensitivity 57%, specicity 71% [41]. A more

recent study that used the invasive angiography as the gold standard,

MDC has shown a good specicity (82-95%) but modest to good

sensitivity (53%-58%). Te lower sensitivity is likely attributable to the

lower spatial resolution o CCA compared with invasive angiography

and presence o plaque calcication [42].

On the other hand, in carotid arteries, the introduction o MDCdid improve the detection o ulceration improving the sensitivity o

single slice C rom 60 to 87% and specicity rom 74 to 98% [43-46].

Plaque composition

By virtue o MDC ability to measure local tissue attenuation,MDC also allows imaging o the vessel wall, potentially providing

insights into plaque composition rather than the physiology [47].

Identification o plaque composition is based on measuring the

attenuation coefficient which is displayed as a C number relative to

the attenuation o water (0 Hounseld units HU) and air (1000 HU)

[48]. Calcications appear as hyperdense, brous tissue as isodense

and lipid core, intra-plaque hemorrhage and thrombus as hypodense.

However, using the absolute C numbers to dene different plaque

constituents, especially o sof plaques, is influenced by various actors

that could limit its accurate assessment, rendering the exact denition

o low attenuation plaque values with the currently available techniques

more challenging. Tese actors include; attenuation o intracoronary

contrast medium, tube voltage, degree o stenosis, use o differentreconstruction lters [49]. able 2 shows some studies that reported

C attenuation values o various coronary plaque types in relation to

IVUS. O note, the reported C numbers showed signicant differences

in densities o plaque components, yet, with substantial overlap.

Coronary artery calcium (CAC) is dened as a hyper-attenuatinglesion >130 HU within an area o 3 pixels. Agatston score has beenwidely used to quantiy CAC scoreby multiplying the lesion area (mm2)by a density actor (between 1 and 4) [54]. CAC score with its clinicaland prognostic implications will be discussed later.

Different classications o morphological patterns o calcicationhave been used in previous reports, one classication was as: speckled(calcied nodules), ragmented (shell-like, linear, or wide, single

ocus o calcium >2 mm in diameter), or diffuse ( 5-mm segmento continuous calcication) [55]. Calcied nodules have been welldescribed on IVUS studies and identied as a less common cause o

Figure 1:A straight-vessel view for the left anterior descending artery with a

proximal plaque. The vessel lumen is measured at the plaque site (B = 4mm)

as well as the proximal (A=3.4mm) and distal (C=3mm) reference segments

demonstrating positive remodeling.

Figure 2: Fig 2A shows a curved multi-planar reformation (MPR) image to the

left anterior descending artery with a proximal plaque. Figs 2B, C and D are

cross section images of the vessel at the plaque site, the criteria of plaque

vulnerability shown are: spotty calcication (arrow 1), low attenuation plaque,

ranging between 14-23 HU (arrow 2) and napkin ring sign (arrow 3).
http://dx.doi.org/10.4172/2329-9495.1000111http://dx.doi.org/10.4172/2329-9495.1000111


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plaque disruption (2-7%). On CCA, Calcied nodules were observedin association with only 6% o obstructive stenotic lesions (>50%),whereas 44% o non-obstructive lesions showed this calcication

pattern [55].

Other studies described classication patterns as spotty anddense calcification. Spotty calcication was dened and sub-classiedaccording to their length on curved multiplanar reconstruction into:small spotty (


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subjects with one or more vulnerability criterion, Moreover; there wasa signicantly higher number o low attenuation plaques and positiveremodeling per subject [75].

Technical Limitations of CTCA

As previously highlighted in table 1, some technical actors might

affect the role o CCA in characterization o coronary plaques.

Tese limitations include: 1) Radiation exposure; typical effective

dose o radiation or retrospectively gated reconstruction is about 15

mSv, radiation doses delivered have markedly reduced to less than 2

mSv with the advent o newer prospective gating and ultra-low-dose

protocols, these advances in technology are expected to urther expand

the CCA applications and would permit ollow-up studies to evaluate

the progression o atherosclerotic plaques over time and with the use

o interventional drugs like statins. 2) contrast agents; currently used

contrast media in CCA are considerably sae, however, there is a

minimal risk that should be anticipated and dealt with in patients with

contrast allergy or those with advanced renal insufficiency. 3) artiacts;

various C artiacts could limit the accuracy o CCA in studying the

plaque composition. O note, dense calcication is a major limiting

actor that could result in the blooming artiact phenomenon where

calcium looks bigger than it actually is and 4) the signicant overlap

between tissue densities as previously discussed, rendering the accurate

denition o plaque constituents more challenging [76].

Future Perspectives and Conclusions

Te concept o vulnerable plaque has been introduced with theintention o detection o those high risk plaques that are potentiallycapable o causing acute cardiac events. Further risk stratication oasymptomatic or previously assumed low risk population is a complexprocess that goes ar and beyond the mere use o risk score calculatorsor blood biomarkers. Tis process has been recently supported bythe rapidly advancing imaging modalities that have shown somecapabilities in visualizing various physical, chemical and biologicalaspects o atherosclerotic plaques that could dene their vulnerability.

Among non-invasive modalities, MDC seems to have the

highest possibility o ullling the expectations o researchers and

clinicians. In addition to its role in assessment o signicant coronary

obstruction with excellent diagnostic accuracy, it is getting popular

as a promising non-invasive tool in detection o vulnerable eatures.

Tis has been supported by studies that showed MDC to have a good

diagnostic accuracy and correlation when compared to histology and

IVUS.A bigger role is expected rom MDC with the development o

higher resolution scanners with lower radiation dose and the use o

novel contrast media that could be targeted towards specic plaque

constituents.

A major question afer the identication o a vulnerable coronary

plaque, should it be treated and how? At present there are no data to

prove that interventional treatment strategies or those high risk but

asymptomatic plaques are superior to conventional medical treatment.

Data rom large prospective studies will be needed to determine which

approach will be benecial.

Finally, we always should remember looking at the big picture

accepting the idea that the pathogenesis o ACS does not involve only

actors operating at the plaque level, but rather there is a concurrence olocal and extra-coronary actors that involve coagulation, neuroendocrine,

inflammatory and immune response o the vascular tissue.

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